Evidence map›Paper›PMID 23465591›Full record

ArticleThe Journal of nutritional biochemistry2013

Protection of nicotinic acid against oxidative stress-induced cell death in hepatocytes contributes to its beneficial effect on alcohol-induced liver injury in mice.

Xiaobing Dou, Chen Shen, Zhigang Wang, Songtao Li, Ximei Zhang, Zhenyuan Song

Open access · greenAbstract read
In one paragraph

Article in The Journal of nutritional biochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
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  15. Diverse therapeutic efficacies and more diverse mechanisms of nicotinamide.Metabolomics : Official journal of the Metabolomic Society · 2019
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 2 countries.

Xiaobing DouCollege of Life Science, Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310053, P R China.
Chen Shen
Zhigang Wang
Songtao Li
Ximei Zhang
Zhenyuan Song
University of Illinois Chicago · USUniversity of Chicago Medical Center · US

Funding

Homocysteine, Adiponectin, and Alcoholic Liver DiseaseR01AA017442 · NIAAA · UNIVERSITY OF ILLINOIS AT CHICAGO · PI SONG, ZHENYUAN · 2009 to 2013
$1.4M
NIAAA NIH HHS R01 AA017442
6 · The paper itself

Abstract

Oxidative stress plays a pathological role in the development of alcoholic liver disease. In this study, we investigated the effects of nicotinic acid (NA) supplementation on H2O2-induced cell death in hepatocytes and alcohol-induced liver injury in mice. Hepatocytes were exposed to H2O2 (0-0.4 mM) for 16 h after a 2-h pretreatment with NA (0-100 μM). Cell viability, intracellular glutathione and total NAD contents were determined. In animal experiments, male C57BL/6 mice were exposed to Lieber-De Carli liquid diet [+/- ethanol with/without NA supplementation (0.5%, w/v) for 4 weeks]. Nicotinic acid phosphoribosyltransferase (NaPRT) is the first enzyme participated in the NA metabolism, converting NA to nicotinic acid mononucleotide (NaMN). In NaPRT-expressing Hep3B cells, H2O2-induced cell death was attenuated by NA, whereas in NaPRT-lost HepG2 cells, only NaMN conferred protective effect, suggesting that NA metabolism is required for its protective action against H2O2. In Hep3B cells, NA supplementation prevented H2O2-inudced declines in intracellular total NAD and GSH/GSSG ratios. Further mechanistic investigations revealed that conservation of Akt activity contributed to NA's protective effect against H2O2-inudced cell death. In alcohol-fed mice, NA supplementation attenuated liver injury induced by chronic alcohol exposure, which was associated with alleviated hepatic lipid peroxidation and increased liver GSH concentrations. In conclusion, our findings indicate that exogenous NA supplementation may be an ideal choice for the treatment of liver diseases that involve oxidative stress.

Indexed as

AnimalsCell DeathGlutathioneHepatocytesHep G2 CellsHumansHydrogen PeroxideLipid PeroxidationLiverLiver Diseases, AlcoholicMaleMiceMice, Inbred C57BLNiacinOxidative StressGlutathioneHydrogen PeroxideNiacinAlcoholGlutathioneHydrogen peroxideLiverNicotinic acidOxidative stress

Identifiers

PMID23465591
PMCPMC3679291
OpenAlexW2078234978

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.